摘要
目的 探讨整合素(INT) β1 局灶黏附激酶(FAK)信号传导通路在侵袭性垂体瘤中的作用及其意义。方法 选取手术切除的新鲜垂体瘤标本8例,进行原代培养,利用Boyden小室侵袭模型,分别加入INTβ1抗体以抑制INTβ1 FAK的激活、加入蛋白激酶C激活剂以激活FAK ,观察干预后垂体瘤细胞中FAK、磷酸化FAK(激活的FAK)、FAKmRNA的变化,以及相应的细胞侵袭能力的变化。结果 在加入INTβ1抗体后,Y3 97 FAK水平明显降低(P <0 .0 5 ) ,FAK的激活被抑制,同时伴随细胞侵袭率的显著降低(P <0 .0 5 ) ;加入蛋白激酶C激活剂后,FAKmRNA水平明显增高(P <0 .0 5 ) ;Y3 97 FAK水平明显增高(P <0 .0 5 ) ,FAK被激活;同时细胞侵袭率增高(P <0 .0 5 )。同时加入INTβ1抗体和TPA后,FAKmRNA水平明显增高(P <0 .0 5 ) ;Y3 97 FAK水平明显增高(P <0 .0 5 ) ,表明FAK仍然被激活,伴细胞侵袭率增高(P <0 .0 5 )。结论 垂体瘤中存在INTβ1 FAK信号传导机制,并且在垂体瘤的侵袭行为中具有重要作用;INTβ1
Objective To explore the possible role of the INTβ1-FAK pathway in the invasion of pituitary adenoma cells primarily cultured in vitro.Methods Eight surgical specimens of pituitary adenomas were collected and underwent primarily culture.INTβ1 antibodies were added into the the cell suspension to inhibit activation of INTβ1-FAK pathway,and phorbel ester TPA was added to activate FAK,and then both were added.Changes of FAK,activated FAK,FAKmRNA and corresponding invasive abilities evaluated with Boyden-chamber model were taken into accounts and the underlying mechanism was discussed.Results When INTβ1 antibodies were added,Y397-FAK was decreased dramatically,accompanied by lower invasive rate ( P < 0.05); When TPA was added,the Y397-FAK level was increased ( P < 0.05), indicating activation of FAK,which was associated with higher invasive rate ( P < 0.05). When both the factors were added,the FAKmRNA level was significantly increased ( P < 0.05), accompanied by higher invasive rate ( P < 0.05). Conclusion The INTβ1-FAK signal pathway plays an important role in the invasive behavior of pituitary adenomas.Some cross-talk mechanism exists between the INTβ1-FAK pathway and protein kinase C pathway.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2005年第4期460-462,共3页
Chinese Journal of Experimental Surgery
基金
国家自然科学基金资助项目 (3 9670 73 6)
